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From the Townsend Letter
June 2010

Remodeling of the Connective Tissue
by Albert Garoli, MD Ay, TCM

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Introduction
The functions of inner biochemical exchange in an organism are fundamental from a metabolic and reparative point of view. Recently, studies have uncovered the inherent capacity of the connective tissue remodeling that can also take place after stimulation of the connective tissue through mechanical, electrical, or thermal means with a predisposed biochemical substratum. Researchers like Katsusuke Serizawa and Dr. Kok Yuen Leung reported the presence of tissue areas endowed with particular thermal and electromagnetic properties especially in conditions of local or systemic phlogosis or after a lesion.1 Local inflamed areas are normally characterized by an elevation of the temperature in the magnitude of 0.2–0.6 grades (Celsius) and might show a diminished electrical resistance down to a 1/100th of the surrounding areas.

Furthermore, Japanese research suggested the presence of electrical flows generated inside the interfascial spaces. Already in 1964, Rokuro Fujita concluded that the muscular movement through serial contraction generates frictions of the fascial planes and that this movement produces weak subcutaneous and periorganic electrical currents.2 The mediation of all reparative effects of the connective tissue through a morphological remodeling is the focus of this article.

The Connective Tissue As a Conveyer of Signal
According to the research of Helene M. Langevin of Vermont University, a transduction mechanism of signals through the connective tissue with an involvement of secondary systems such as the PNS (peripheral nervous system) could explain how a mechanical stimulation could induce biochemical tissue changes.3

The transmission of the signal, based on a serial systematic contraction of the connected areas with a kinetic-dynamic modality, constitutes the best explanation of the phenomena of biological signaling" mediated by low electrical currents.

The most responsive tissue to mechanical endogenous and exogenous stimuli is without any doubt the fascial connective tissue, an avascular system constituted predominantly by collagen and glycosaminoglycans (GAGs) and proteoglycans (PGs).

Collagen constitutes 25% to 35% of the total proteic content of the organism and endows the tissues with a characteristic resistance to traction, typical of tissues such as tendons and fasciae. Collagens like types I, II, and III are called fibrillar collagens due to their capacity to assemble in fibrils shaped like cables and are those that interest the researcher from a signaling point of view. Fasciae are composed of fibers endowed with strong elasticity but also great responsivity to climatic, environmental, electromagnetic, thermal, biochemical, and neuroendocrine variations.

The facial tissue constitutes the bridge between milieu interieur and milieu exterieur, as well as a system of signal transduction that correlates the organism with its environment. Climatic and temperature changes can influence tone and morphology of the interstitial and fascial connective tissue.

The orientation of fasciae is predominantly longitudinal and allows a total connectivity, an immediate reactivity to all stimuli, and a multifactorial adaptive capacity to all changes of homeostasis in the body. Anatomofunctional alterations of this tissue thus might correspond with changes in interstitial electrical flow and altered biochemical content. Furthermore, fascial hypotonus might contribute to prolapses and delayed muscular response, while the rich nervous presence in the fascial tissue allows strong reactivity to multifactorial stimuli:
  1. pain through nociceptors
  2. pressure and vibration through mechanoreceptors
  3. variation of temperature through thermoreceptors
  4. variations of tone and movement through proprioceptors
  5. variation of biochemical environment through chemoreceptors

The Lesion
After injury, fascial tissues enter a typical phase of remodeling. A lab study investigated samples from normal autoptic fascia lata tissue of 23 individuals devoid of any lesion and another 23 samples from patients operated on after a femoral fracture.4 Tissues obtained where divided in two classes, according to individuation of GAG and individuation of PG. GAGs were extracted through papain digestion and fractioned through cetylpyridinium chlorate. PGs were extracted using 4M guanidine HCl.  The test showed a high content of GAGs in the injured fascia. Results indicated that a lesion is followed by a quantitative and qualitative alteration of the ratio of GAGs and PGs. Morphological modifications of an injured tissue can induce an excess of mucopolysaccharides (GAG) and thus an edematous state, given the hydrophilic properties of these molecules. In the states that precede the lesion, we can hypothesize a chronic contractile state and a dehydration of the tissue coinciding with a molecular gelification. In a state of gelification, fascia and elastic tissues shorten and adhere reciprocally, thus increasing in density and rigidity. The fascia then enters a state of solubilization when its biochemical structure changes through augmented perfusion of liquids.

Remodeling
Remodeling of the connective tissue is induced by an anabolic mechanism and mediated by a tensile or contractile state. When a contraction of the tissue is prolonged, a state of hypertonus takes place and the tissue responds with the production of new molecular material constituted by proteins and mucopolysaccharides, through secretion of collagen from fibroblasts and other molecular components elaborated by the extracellular matrix (ECM). This material creates tissues that are less elastic and thicker, creating inhibition of movement and increasing the contractile strength in a tissue that is already hypertonic.
                                                  
Sensitivity to Biochemical Conditions
The response of the fascial tissue to exogenous and endogenous signals consists of a contraction, a release, and a stable morphological variation of the same tissue through a variation of its molecular components. Remodeling is strongly influenced by factors such as the activity of chemoreceptors, circulating hormones, content of ascorbic acid (vitamin C) for all collagen type I, content of calcium, and external temperature. The phases of solubilization and gelification of the PGs and GAGs components are also sensitive to chronobiological fluctuation such as circadian and annual biorhythms.

It is widely known that estroprogestinic hormones in the female produce a change of tone in uterine fasciae and the ligaments of the lower limb. It has also been demonstrated a higher probability of lesion of the anterior cruciate ligament in women during the ovulatory phase.5,6

Conclusions
Through mechanical means, the contractile fascial impulse can be interrupted and modulated for a time sufficient to allow the tissue to enter a phase of inverse remodeling, thus recomposing structure and tone, augmenting intrafascial electrical flow and the drainage of proteic material released in the phase of buildup. This material can later be reduced through ingestion by macrophages in the ECM. With the effect of proprioceptive compensation in the mechanical treatment of the connective tissue, tensions can be released and transduced in a biphasic tonic signal. The mechanical stimulation of the Golgi tendon organs neurofascial feedback can also be modulated, producing relaxation of tissues to avoid excessive tension. Furthermore, the mechanical stimulation of Pacini's corpuscles, detecting change in pressure and vibration, can initiate a relaxing response. These deep fasciae can be relaxed through regular and slow stretching and mechanoinduction of Ruffini's endings, spindle-shaped receptors sensitive to skin stretch. This last stimulation can elicit an inhibition of sympathetic activity, indirectly reducing heartbeat and respiratory rhythm. Hence, proprioceptive stimulation can take place specifically if the correct biochemical and external environments are maintained.

Notes

1. Oshima Y, Takahashi K, Serizawa K, Fujita T, Kubota T, Mori K. Individual pattern changes in the distribution of skin temperature, electric resistance, and potential difference. Department of Physical Therapy & Medicine, School of Medicine, University of Tokyo & Institute of Physical Therapeutics, Tokyo University of Education. Study read at: 4th International Congress of Physical Medicine in Paris; 1964.
2. Fujita R. Study on meridians, 1st and 2nd reports. Paper presented at: Japan Society for Oriental Medicine in Japan; 1952.
3. Langevin HM, Yandow JA. Relationship of acupuncture points and meridians to connective tissue planes. Presented at: Department of Neurology, University of Vermont College of Medicine, Burlington, VT; 1998
4. Kozacutema EM, Olczyk K, Glstrokowacki A, Bobinacuteski R. An accumulation of proteoglycans in scarred fascia. Mol Cell Biochem.2000:203(1–2):103–112(10).
5. Chaudhari, AMW, Zelman EA, Flanigan DC, Kaeding CC, Nagaraja HN. Anterior cruciate ligament-injured subjects have smaller anterior cruciate ligaments than matched controls: a magnetic resonance imaging study. Am J Sports Med. 2009;37(12):1282–1285
6. Park S-K, Stefanyshyn DJ, Loitz-Ramage B, Hart DA, Ronsky JL.  Changing hormone levels during the menstrual cycle affect knee laxity and stiffness in healthy female subjects. Am J Sports Med. 2009:37(3):588–598

Albert Garoli is a proficient health practitioner, medical researcher, and educator. He is a specialist in Ayurvedic medicine, Traditional Chinese Medicine, acupuncture, herbology, biophysics, and homotoxicology. Currently, he is teaching in the Italian College of Osteopathy (CIO) as well as the Italian School for Oriental Medicine (ScuolaTao), in convention with University Sapienza of Rome. He is also the director of the Holonomics cooperative project. His many years of experience have brought him to a revolutionary understanding of human neurobiology, which is clearly explained in his new book, The Evolutionary Glitch. For more information, go to www.theevolutionaryglitch.com, or e-mail admin@theevolutionaryglitch.com.

 

 

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